Metallic glasses, now that many compositions can be made in bulk, are of interest for structural applications exploiting their yield stress and yield strain, which are exceptionally high for metallic materials. Their applicability is limited by their near-zero tensile ductility resulting from work-softening and shear localization. Even though metallic glasses can show extensive local plasticity, macroscopically they can effectively be brittle, and much current research is directed at improving their general plasticity. In conventional engineering materials as diverse as silicate glasses and metallic alloys, we can improve mechanical properties by the controlled introduction of compressive surface stresses. Here we demonstrate that we can controllably induce such residual stresses in a bulk metallic glass, and that they improve the mechanical performance, in particular the plasticity, but that the mechanisms underlying the improvements are distinct from those operating in conventional materials.

Aim: To explore the physiological consequences of the ryanodine receptor (RyR2)-P2328S mutation associated with catecholaminergic polymorphic ventricular tachycardia (CPVT s/s hearts showed higher incidences of nsVTs before but mainly sVTs after introduction of isoproterenol with both regular stimuli and PES, particularly at higher pacing frequencies. Additionally, intrinsically beating RyR2 s/s showed extrasystolic events often followed by spontaneous sVT. Conclusion:The RyR2-P2328S mutation results in marked alterations in cellular Ca 2+ homeostasis and arrhythmogenic properties resembling CPVT with greater effects in the homozygote than the heterozygote demonstrating an important gene dosage effect.

These results suggest that abnormal intracellular Ca(2+) homoeostasis produces both arrhythmic triggers and a slow-conducting arrhythmic substrate in RyR2(S/S) atria. A similar mechanism might also contribute to arrhythmogenesis in other conditions, associated with diastolic Ca(2+) release, such as atrial fibrillation.

We describe a method of reducing threading dislocation densities in 0001-oriented GaN from (5.0±0.5)×109cm−2to(3.1±0.4)×107cm−2 (for coalesced films) or to below 5×106cm−2 (for partially coalesced films) in a single step, without lithography. Lattice-matched, dislocation-blocking scandium nitride interlayers are deposited on a 500nm GaN-on-sapphire template. Dislocation-free GaN islands grown on the ScN interlayer nucleate both on the interlayer and on tiny areas of the GaN template exposed through openings in the interlayer. However, some dislocations are generated above the interlayer during subsequent island coalescence.